Clemizole sulfate
Clemizole sulfate is an orally active, blood-brain barrier permeable TRPC5 inhibitor, with an IC50 value of 1.05-1.34 μM against mouse TRPC5. Clemizole sulfate blocks TRPC1:TRPC5, TRPC3, TRPC4, TRPC6, TRPC7, hERG, hKCNQ1/hKCNE1 and hKv1.5 channels, and activates TRPA1; it modulates 5HT-2B and HTR2A receptors; it inhibits HCV RNA replication, CrtN enzymatic activity, oxidative stress, neuroinflammation, cell apoptosis and bacterial virulence; it maintains blood-brain barrier (BBB) integrity; it enhances DNA repair capacity; it improves cell viability; and it alters cardiac electrophysiological properties. Clemizole sulfate can be used in the research of Dravet syndrome, hepatitis C virus infection, Staphylococcus aureus skin infection, Cisplatin (HY-17394)-induced nephrotoxicity, STXBP1-related diseases, traumatic brain injury and xeroderma pigmentosum type C.
For research use only. We do not sell to patients.
- CAS No.: 17162-20-8
- Formula: C19H22ClN3O4S
- Molecular Weight:423.91
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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TRPC5 1.05-1.34 μM (IC50) |
Clemizole sulfate exhibits strong, synergistic anti-HCV activity in Huh 7.5 cells when combined with Boceprevir (HY-10237), with a synergy volume of 230 μM2%, and does not induce cellular toxicity at tested concentrations[9].
Clemizole sulfate (as Clemizole Hydrochloride) (1-10 μM; 24 h) significantly increases the viability of XP-C patient-derived fibroblasts exposed to UVB irradiation, with a dose-dependent protective effect that enhances photo-resistance compared to DMSO-treated cells[11].
Clemizole sulfate (as Clemizole Hydrochloride) (5 μM; 24 h) significantly promotes repair of UVB-induced 6-4PP DNA lesions in XP-C patient-derived fibroblasts[11].
Clemizole sulfate (as Clemizole Hydrochloride) (0.1-10 μM; 24 h) mediates enhanced UVB photo-resistance in XP-C patient-derived fibroblasts through both pre- and post-UVB irradiation treatment, with the combined regimen yielding the highest bioactivity[11].
Clemizole sulfate (as Clemizole Hydrochloride) (10 μM; 2-4 h) does not affect DNA replication or cell proliferation in XP-C patient-derived fibroblasts exposed to UVB irradiation[11].
Clemizole sulfate (as Clemizole Hydrochloride) (10 μM; 24 h) does not reduce apoptosis or necrosis to mediate its protective effect in XP-C patient-derived fibroblasts exposed to UVB irradiation[11].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Xeroderma Pigmentosum C (XP-C) patient-derived immortalized fibroblasts (GM15983)
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Concentration:10 μM (24 h pre-irradiation treatment); 10 μM (24 h post-irradiation treatment); 1-10 μM (both pre- and post-irradiation treatments)
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Incubation Time:24 h (pre-irradiation treatment); 24 h (post-irradiation treatment)
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Result:Showed ≥25% photo-resistance and a robust Z score above 2.6 in primary screen.
Induced a significant 20 to 40% increase in XP-C cell viability depending on UVB dose and reagent concentration, with increased bioactivity at higher concentrations.
Significantly enhanced photo-resistance in XP-C cells across increasing UVB doses, with viability remaining higher than DMSO-treated controls at all tested UVB doses.
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Cell Line:Xeroderma Pigmentosum C (XP-C) patient-derived immortalized fibroblasts (GM15983)
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Concentration:0.1-10 μM (pre-irradiation only; post-irradiation only; combined pre- and post-irradiation treatments)
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Incubation Time:24 h post-UV
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Result:Reached ~20% increased cell viability at 10 μM with pre-irradiation treatment alone.
Reached an average of ~50% increased viability at 10 μM with post-irradiation treatment alone.
Showed the highest bioactivity with combined pre- and post-irradiation treatment, with a significant increase compared to pre-treatment alone at both 5 μM and 10 μM, and no significant difference compared to post-treatment alone.
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Cell Line:Xeroderma Pigmentosum C (XP-C) patient-derived immortalized fibroblasts (GM15983)
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Concentration:10 μM (both pre- and post-irradiation treatments)
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Incubation Time:2 h post-UV; 4 h post-UV
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Result:Showed no significant increase in EdU mean fluorescence intensity (MFI) compared to DMSO-treated cells at 2 h or 4 h post-UV.
Showed no significant difference in the percentage of EdU-positive cells from DMSO-treated cells at either time point, indicating no enhancement of DNA replication or cell proliferation.
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Cell Line:Xeroderma Pigmentosum C (XP-C) patient-derived immortalized fibroblasts (GM15983)
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Concentration:10 μM (both pre- and post-irradiation treatments)
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Incubation Time:24 h post-UV incubation
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Result:Did not show a significant decrease in apoptotic (CellEvent-positive) or necrotic (PI-positive) cell populations compared to DMSO-treated cells.
Did not significantly increase the live cell population.
Clemizole (100-400 μM; p.o.; 30-min exposure; 90-min exposure) sulfate suppresses seizure-associated locomotion in scn1Lab mutant zebrafish larvae at doses of 100 μM (90-min exposure), 300 μM, and 400 μM (30-min exposure), with toxicity observed at higher concentrations during prolonged exposure[10].
Clemizole (250 μM; p.o.; single exposure) sulfate significantly suppresses seizure-associated locomotion in scn1Laa mutant zebrafish larvae, a second Dravet syndrome model[10].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley Rat (6-8 weeks old)[8]
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Dosage:10 mg/kg; 30 mg/kg
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Administration:i.p.; single dose
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Result:Promoted neurological function recovery after TBI in a dose-dependent manner.
Improved sensorimotor dysfunction after TBI.
Reversed TBI-related anxiety-like behaviors.
Improved spatial learning and memory deficits after TBI without affecting motor function.
Alleviated TBI-induced oxidative stress and restored antioxidant defense capabilities.
Alleviated TBI-induced cortical cell damage.
Inhibited microglia and astrocyte activation, reduced pro-inflammatory cytokine levels, and restored tight junction protein expression, thus protecting the integrity of the blood-brain barrier.
Activated the PI3K-Akt pro-survival pathway, downregulated the Bax/Bcl-2 ratio, and inhibited the caspase cascade, thus exerting an anti-apoptotic effect.
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Animal Model:TL strain (5 days post fertilization, undifferentiated sex)[10]
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Dosage:100 μM (90-min exposure); 300 μM (30-min exposure); 400 μM (30-min exposure)
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Administration:p.o.; 30-min exposure; 90-min exposure
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Result:Suppressed seizure-related locomotion at 300 μM and 400 μM (30-min exposure) and at 100 μM (90-min exposure), reducing mean swim velocity by ≥40%.
Caused toxicity at 300 μM and 400 μM during prolonged 90-min exposure.
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Animal Model:TL strain (5 days post fertilization, undifferentiated sex)[10]
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Dosage:250 μM
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Administration:p.o.; single exposure
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Result:Significantly reduced mean swim velocity in scn1Laa mutant larvae, suppressing seizure behaviour similarly to known antiepileptic agents stiripentol and diazepam.
Chemical Information
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CAS No. 17162-20-8
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Molecular Weight 423.91
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Formula C19H22ClN3O4S
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SMILES
O=S(O)(O)=O.ClC1=CC=C(CN2C3=C(N=C2CN4CCCC4)C=CC=C3)C=C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Richter JM, et al. Clemizole hydrochloride is a novel and potent inhibitor of transient receptor potential channel TRPC5. Molecular pharmacology. 2014 Nov;86(5):514-21. [Content Brief]
[2]. Baraban SC, et al. Drug screening in Scn1a zebrafish mutant identifies clemizole as a potential Dravet syndrome treatment. Nature communications. 2013;4:2410. [Content Brief]
[3]. Jie LJ, et al. Clemizole hydrochloride blocks cardiac potassium currents stably expressed in HEK 293 cells. British journal of pharmacology. 2017 Feb;174(3):254-266. [Content Brief]
[4]. Einav S, et al. Discovery of a hepatitis C target and its pharmacological inhibitors by microfluidic affinity analysis. Nature biotechnology. 2008 Sep;26(9):1019-27. [Content Brief]
[5]. Yu H, et al. Clemizole inhibits CrtN-driven staphyloxanthin biosynthesis in Staphylococcus aureus to enhance host immune clearance. Communications biology. 2026 Feb 25;9(1):484. [Content Brief]
[6]. Kumaş-Kulualp M, et al. Clemizole hydrochloride, a potent TRPC5 calcium channel inhibitor, prevents cisplatin-induced nephrotoxicity in Spraque-Dawley rats. Journal of biochemical and molecular toxicology. 2023 Jul;37(7):e23372. [Content Brief]
[7]. Moog M, et al. Clemizole and trazodone are effective antiseizure treatments in a zebrafish model of STXBP1 disorder. Epilepsia open. 2022 Sep;7(3):504-511. [Content Brief]
[8]. Chauhan C, et al. Clemizole Mitigates Traumatic Brain Injury by Inhibiting Oxidative Stress, Neuroinflammation, and Apoptosis. ACS chemical neuroscience. 2026 May 06;17(9):1787-1801. [Content Brief]
[9]. Nishimura T, et al. Using chimeric mice with humanized livers to predict human drug metabolism and a drug-drug interaction. The Journal of pharmacology and experimental therapeutics. 2013 Feb;344(2):388-96. [Content Brief]
[10]. Griffin A, et al. Clemizole and modulators of serotonin signalling suppress seizures in Dravet syndrome. Brain : a journal of neurology. 2017 Mar 01;140(3):669-683. [Content Brief]
[11]. Kobaisi F, et al. Isoconazole and Clemizole Hydrochloride Partially Reverse the Xeroderma Pigmentosum C Phenotype. International journal of molecular sciences. 2021 Jul 29;22(15):8156. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Clemizole sulfate Related Classifications
HY-30234B Related Classifications
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